羧基化柚子皮吸附Cd^(2+)的性能与机制

为探索利用食品加工废弃物柚子皮制备一种重金属离子吸附材料的可行性,通过NaOH将柚子皮中甲酯化的羧基水解成羧酸,再利用TEMPO/次氯酸钠/溴化钠体系将柚子皮中C-6位伯羟基氧化成羧酸,制备出一种羧基化柚子皮吸附材料,同时采用FTIR、SEM-EDS和XPS对柚子皮和吸附Cd^(2+)前后的羧基化柚子皮进行表征,研究其吸附机制。结果表明羧基化柚子皮中羧基含量为2.34 mmol/g,是改性前的10.64倍,且可以有效地去除水溶液中Cd^(2+)。羧基化柚子皮吸附Cd^(2+)更符合Langmuir和伪二阶动力学模型,属于单层化学吸附,对Cd^(2+)的最大吸附量为76.16 mg/g,是改性前的5.81倍。羧基化柚子皮中羧基(-COO^(-))是吸附Cd^(2+)的功能性基团,吸附后形成羧酸镉,其中镉以Cd^(2+)的形式存在,与-COO^(-)的配位方式主要是双齿桥式,该吸附过程是一个阳离子(Na^(+)和Cd^(2+))交换的过程。

好氧堆肥对生物炭理化性质及吸附Cd^(2+)稳定性的影响

生物炭可作为畜禽粪污好氧堆肥中去除重金属的功能材料,但堆体内部复杂的环境变化会影响生物炭的理化性质,从而影响其对重金属吸附的稳定性。将普通秸秆生物炭(BC)和磁性秸秆生物炭(FBC)置于牛粪中进行30 d好氧堆肥试验,研究两种生物炭基本理化性质及对Cd^(2+)吸附稳定性的影响。结果表明:堆肥处理使BC和FBC的比表面积分别增加20.56%和76.64%,总孔容分别下降2.36%和3.70%,平均孔径分别下降19.17%和46.54%,表面官能团发生变化,FBC的饱和磁化强度下降43.67%。堆肥后,饱和吸附Cd^(2+)的两种生物炭BC和FBC的TCLP提取态Cd(TCLP-Cd)占比和TCLP提取液pH(TCLP-pH)均呈下降趋势,其中TCLP-Cd占比分别从28.31%和22.85%显著下降至26.76%和13.85%(P<0.05),TCLP-pH分别从3.66和3.29显著下降至3.51和3.14。综上,堆肥老化改变了两种生物炭的理化性质,降低了其酸可提取态Cd的含量,提高了其吸附Cd 2+的稳定性,且FBC中Cd^(2+)的稳定性更强。

羧甲基改性沙柳木粉膜吸附Cd^(2+)的性能研究

沙柳木粉(SPP)经醚化反应制备成羧甲基沙柳木粉(CMS)。将CMS溶解到1-丙烯基-3-甲基咪唑氯盐(AMIMJCI)和二甲基亚砜(DMSO)中,采用聚乙烯醇(PVA)为成膜剂,制备羧甲基沙柳木粉膜(CMSM)。探究在不同吸附条件下CMSM对Cd^(2+)的吸附性能。采用FTIR、SEM、XRD和XPS对CMSM进行表征。吸附结果表明:Cd^(2+)初始浓度为800mg·L^(-1),pH值为5,吸附时间105min,吸附温度35℃时,CMSM对Cd^(2+)的吸附效果最佳。表征结果表明:0-H、-COOH、-C-O-C-、-CH_(2)、-NH_(2),基团参与吸附Cd^(2+)的反应。CMSM表面比较疏松,有孔隙,成狭缝型。CMSM晶体内部变得蓬松,Cd^(2+)更容易被CMSM吸附。CMSM对Cd^(2+)的吸附属于多分子层吸附,同时存在化学吸附和物理吸附,且以化学吸附为主,准二级动力学模型和Freundlich等温线模型与其吸附过程相符合。

农业废弃物生物炭制备及其对Cd^(2+)的吸附特征

[目的]本文旨在探讨不同农业废弃物生物炭对Cd^(2+)的吸附特征,为农业废弃物资源化利用以及环境中Cd^(2+)的修复提供理论依据和技术支撑。[方法]本研究以农业废弃物为原料,平菇菌渣、香菇菌渣、玉米秸秆、牛粪分别在300、400、500℃温度下限氧热解反应制备3种平菇菌渣生物炭(PGBC)、3种香菇菌渣生物炭(XGBC)、3种牛粪生物炭(NFBC)和3种玉米秸秆生物炭(YMBC)共12种生物炭,并对吸附性能最好的500℃下热解制备的平菇生物炭PG500进行铁锰复合改性(FM-PG500)。采用BET、FTIR等方法对制备生物炭理化特性进行表征,开展吸附试验研究不同物源和铁锰复合改性生物炭对Cd^(2+)的吸附性能及特征。[结果]随着热解温度的提高,4种生物炭的产率均随之减小,灰分含量、比表面积及孔容呈相反变化趋势;芳香族官能团相对含量增加,其结构趋于稳定,且铁锰复合改性后的FM-PG500具备最高的芳香化程度。PG500对Cd^(2+)吸附量最高。不同农业废弃物生物炭对Cd^(2+)的吸附过程均符合准二级动力学,其中PGBC、XGBC和FM-PG500拟合结果符合Langmuir模型,为单分子层化学吸附,而YMBC和NFBC符合Freundlich模型,为多分子层的化学吸附。在吸附热力学实验中,当Cd^(2+)浓度为10~80 mg·L^(-1)时,FM-PG500的平衡吸附量由未改性前的4.96~36.52 mg·g^(-1)提高至5.41~38.04 mg·g^(-1);吸附动力学实验中,当Cd^(2+)浓度为20 mg L^(-1)时,FM-PG500对Cd^(2+)的吸附量相较于未改性前提升了11.0%。[结论]平菇菌渣作为原材料制备生物炭对水中Cd^(2+)的去除有较大潜力,铁锰氧化物负载之后改变了生物炭的理化性质从而有利于生物炭吸附性能的提高。

Involvement of the ABA-and H_(2)O_(2)-Mediated Ascorbate-Glutathione Cycle in the Drought Stress Responses of Wheat Roots

Abscisic acid(ABA),hydrogen peroxide(H_(2)O_(2)) and ascorbate(AsA)–glutathione(GSH)cycle are widely known for their participation in various stresses.However,the relationship between ABA and H_(2)O_(2) levels and the AsA–GSH cycle under drought stress in wheat has not been studied.In this study,a hydroponic experiment was conducted in wheat seedlings subjected to 15%polyethylene glycol(PEG)6000–induced dehydration.Drought stress caused the rapid accumulation of endogenous ABA and H_(2)O_(2) and significantly decreased the number of root tips compared with the control.The application of ABA significantly increased the number of root tips,whereas the application of H_(2)O_(2) markedly reduced the number of root tips,compared with that under 15%PEG-6000.In addition,drought stress markedly increased the DHA,GSH and GSSG levels,but decreased the AsA levels,AsA/DHA and GSH/GSSG ratios compared with those in the control.The activities of the four enzymes in the AsA–GSH cycle were also markedly increased under drought stress,including glutathione reductase(GR),ascorbate peroxidase(APX),monodehydroascorbate reductase(MDHAR)and dehydroascorbate reductase(DHAR),compared with those in the control.However,the application of an ABA inhibitor significantly inhibited GR,DHAR and APX activities,whereas the application of an H_(2)O_(2) inhibitor significantly inhibited DHAR and MDHAR activities.Furthermore,the application of ABA inhibitor significantly promoted the increases of H_(2)O_(2) and the application of H_(2)O_(2) inhibitor significantly blocked the increases of ABA,compared with those under 15% PEG-6000.Taken together,the results indicated that ABA and H_(2)O_(2) probably interact under drought stress in wheat;and both of them can mediate drought stress by modulating the enzymes in AsA–GSH cycle,where ABA acts as the main regulator of GR,DHAR,and APX activities,and H_(2)O_(2) acts as the main regulator of DHAR and MDHAR activities.

电化学快速合成UiO-66及构建电化学传感器检测Cd^(2+)

由于目前合成UiO-66需要高温和长时的苛刻条件,本文采用电化学方法,在无需添加锆盐、常温和2 h的条件下快速合成出UiO-66,并用其制备UiO-66/玻碳电极(GCE)构建电化学传感器检测Cd^(2+)。通过扫描电子显微镜(SEM)、傅立叶红外光谱(FT-IR)、 X射线衍射(XRD)和比表面积(BET)的表征及分析可知,合成的UiO-66为菱形十二面体结构,结晶度良好,比表面积较大,可达到1 054.455 m^(2)/g,总孔隙体积为0.709 cm3/g。同时,探索出最佳检测条件为:NaAc-HAc缓冲溶液pH值为5、富集电压为-1.0 V、富集时间为120 s。在最佳检测条件下,基于UiO-66构建的电化学传感器对Cd~(2+)的检测灵敏度为4.10 AM^(-1),最低检测限为0.037μM,显示出较好的检测Cd^(2+)性能,并且具有良好的重现性、稳定性和抗干扰性。回收实验表明,检测实际汾河水样效果良好。

Duodenal-jejunal bypass improves hypothalamic oxidative stress and inflammation in diabetic rats via glucagon-like peptide 1-mediated Nrf2/HO-1 signaling

BACKGROUND Type 2 diabetes mellitus(T2DM)is often accompanied by impaired glucose utilization in the brain,leading to oxidative stress,neuronal cell injury and inflammation.Previous studies have shown that duodenal jejunal bypass(DJB)surgery significantly improves brain glucose metabolism in T2DM rats,the role and the metabolism of DJB in improving brain oxidative stress and inflammation condition in T2DM rats remain unclear.AIM To investigate the role and metabolism of DJB in improving hypothalamic oxidative stress and inflammation condition in T2DM rats.METHODS A T2DM rat model was induced via a high-glucose and high-fat diet,combined with a low-dose streptozotocin injection.T2DM rats were divided into DJB operation and Sham operation groups.DJB surgical intervention was carried out on T2DM rats.The differential expression of hypothalamic proteins was analyzed using quantitative proteomics analysis.Proteins related to oxidative stress,inflammation,and neuronal injury in the hypothalamus of T2DM rats were analyzed by flow cytometry,quantitative real-time PCR,Western blotting,and immunofluorescence.RESULTS Quantitative proteomics analysis showed significant differences in proteins related to oxidative stress,inflammation,and neuronal injury in the hypothalamus of rats with T2DM-DJB after DJB surgery,compared to the T2DM-Sham groups of rats.Oxidative stress-related proteins(glucagon-like peptide 1 receptor,Nrf2,and HO-1)were significantly increased(P<0.05)in the hypothalamus of rats with T2DM after DJB surgery.DJB surgery significantly reduced(P<0.05)hypothalamic inflammation in T2DM rats by inhibiting the activation of NF-κB and decreasing the expression of interleukin(IL)-1βand IL-6.DJB surgery significantly reduced(P<0.05)the expression of factors related to neuronal injury(glial fibrillary acidic protein and Caspase-3)in the hypothalamus of T2DM rats and upregulated(P<0.05)the expression of neuroprotective factors(C-fos,Ki67,Bcl-2,and BDNF),thereby reducing hypothalamic injury in T2DM rats.CONCLUSION DJB surgery improve oxidative stress and inflammation in the hypothalamus of T2DM rats and reduce neuronal cell injury by activating the glucagon-like peptide 1 receptor-mediated Nrf2/HO-1 signaling pathway.

课程实践融入《试验设计与数据处理》教学--改性花生壳吸附剂的制备及其对重金属Cd^(2+)的吸附性能研究

随着我国提出新工科建设路线,结合地方高校(贺州学院)的地域特色和应用型人才的培养目标,本文通过课程考核形式,设计一个利用花生壳为原料制备出改性花生壳吸附剂(MPS)的试验。学生通过对吸附剂的合成、表征、试验设计和数据分析等环节,将《试验设计与数据处理》课程中所学知识应用到实际试验中,加深对课程知识的理解,锻炼其实际应用能力。

Cd^(2+)浓度对好氧颗粒污泥EPS各组分形成的影响

为探究重金属Cd^(2+)对好氧颗粒污泥系统运行的影响,采用紫外分析法和三维荧光光谱分析法研究了SBR反应器中不同浓度的重金属Cd^(2+)对好氧颗粒污泥EPS总量以及各组分(LB-EPS、SB-EPS、TB-EPS)的产生与组成成分的影响。试验结果表明:低浓度Cd^(2+)(小于0.1mg/L)促进EPS的产生,高浓度Cd^(2+)(大于3mg/L)抑制EPS的产生;SB-EPS随着Cd^(2+)浓度的增加逐渐减少,其中蛋白质含量增加,多糖、腐殖酸明显减少;当Cd^(2+)浓度小于0.1mg/L时TB-EPS显著增加,其中主要增加的成分是蛋白质;当Cd^(2+)浓度大于3mg/L时,TB-EPS的分泌受到抑制,但蛋白质含量仍高于空白对照组,多糖、腐殖酸含量显著降低;LB-EPS受到的影响因素较多,其含量变化不规律。采用扩展DLVO理论剖析了EPS各组分含量的变化对好氧颗粒污泥沉降性能的影响,以期为好氧颗粒化技术在工业废水处理中的应用提供有力的支持。

虾青素对镉离子(Cd^(2+))诱导下斑马鱼胚胎抗氧化指标的影响

(28.0±0.5)℃下,将100个产后1 h的斑马鱼(Danio rerio)胚胎放在120 mm培养皿中,暴露在<0.02%浓度的二甲基亚砜(DMSO,对照组)、50μg/L Cd^(2+)(低浓度暴露组)、500μg/L Cd^(2+)(高浓度暴露组)和Cd^(2+)+雨生红球藻(Haematococcus pluvialis)虾青素AST联合暴露组(50μg/L Cd^(2+)+100μg/L AST组和500μg/L Cd^(2+)+100μg/L AST组)5个处理组中,120 h后测定斑马鱼幼鱼活性氧(ROS)、丙二醛(MDA)和谷胱甘肽酶(GSH)含量、超氧化物歧化酶(SOD)活性和总抗氧化能力(T-AOC),研究重金属镉离子(Cd^(2+))暴露下斑马鱼胚胎的抗氧化响应,探讨AST对斑马鱼机体氧化损伤的缓解效果。结果表明,斑马鱼胚胎Cd^(2+)暴露120 h后,体内活性氧(ROS)和丙二醛(MDA)含量随着Cd^(2+)浓度的升高而增加;GSH含量、SOD和T-AOC的活性随着Cd^(2+)浓度的增加而降低。说明Cd^(2+)可诱导斑马鱼机体出现氧化应激和氧化损伤。添加AST后,斑马鱼幼鱼体内ROS和MDA含量下降,GSH含量、SOD和T-AOC活性上升,说明添加AST可在一定程度上缓解重金属Cd^(2+)对斑马鱼体内抗氧化指标的负面影响。本研究结果可为AST作为新型鱼类饲料添加剂提供理论依据。

粉煤灰基P型沸石吸附水中Cu^(2+)和Cd^(2+)

以粉煤灰(FA)为原料经水热反应合成了P型沸石(Z-P).采用X射线荧光光谱仪、X射线衍射仪、场发射环境扫描电子显微镜、比表面孔径分析仪、傅里叶变换红外光谱仪和X射线光电子能谱对Z-P进行表征,并研究了其对Cu^(2+)和Cd^(2+)的吸附性能.结果表明,Z-P的BET比表面积和孔隙体积分别为38.46m^(2)/g和0.2180cm^(3)/g,均高于FA的1.273m^(2)/g和0.0120cm^(3)/g.FA、Z-P对Cu^(2+)和Cd^(2+)的吸附更符合拟二级动力学模型和Langmuir等温线模型.Z-P对Cu^(2+)和Cd^(2+)的最大吸附量分别为157.48,131.57mg/g,远高于于FA的30.88,25.47mg/g.Z-P对Cd^(2+)的循环再生吸附效果好,但对Cu^(2+)的循环再生吸附效果较差.离子强度对Z-P吸附Cu^(2+)和Cd^(2+)分别起促进和抑制作用.表明Z-P可以作为有效且廉价的Cu^(2+)、Cd^(2+)吸附剂,为FA的资源化利用和含Cu^(2+)、Cd^(2+)重金属离子废水吸附剂的开发提供了一种方法.

硝酸改性显著提高花生壳生物炭对Cd^(2+)的去除能力

本研究采用热分解的方法制备花生壳生物炭,并用乙醇、硝酸和高锰酸钾溶液对其进行改性。分别研究不同方法改性后生物炭吸附Cd^(2+)的性能对初始浓度、吸附时间和pH的响应特征并通过吸附热力学和动力学探索吸附机理。结果表明,改性后的花生壳生物炭对Cd^(2+)的吸附量和去除率明显提高。在花生壳投加量一定的情况下,综合分析得知硝酸改性后对Cd2+吸附效果最佳,吸附量为48.47 mg/g,去除率为96.94%。最佳条件为:Cd^(2+)初始浓度200 mg/L,pH为7,吸附时间120 min。

半焦条件优化对油页岩Cd^(2+)、Pb^(2+)吸附性能的影响

为深入研究温度对半焦油页岩Cd^(2+)、Pb^(2+)吸附性能的影响,以新疆巴里坤矿区油页岩(oil shale,OS)渣为原料,在200~800℃下半焦改性,制备出4种半焦油页岩(OS-200、OS-400、OS-600、OS-800)。使用扫描电子显微镜(scanning electron microscope,SEM)、透射电子显微镜(transmission electron microscope,TEM)、热重分析(thermogravimetric analysis,TGA)、X射线衍射分析(X-ray diffraction,XRD)、比表面积分析方法BET(Brunauer-Emmett-Teller)和傅里叶变换红外光谱分析(Fourier transform infrared spectroscopy,FTIR)等技术进行了物相表征,通过吸附试验研究了其对Cd^(2+)、Pb^(2+)的吸附性能。结果表明:通过不同温度的焦化,OS的物理性状、热重特性等均发生明显变化,在未改变其基本矿物成分的基础上改变了—OH、C O和Si—O—Si化学键的活性,增加了其比表面积。OS-600表现出更好的吸附性能,在pH=7,25℃的条件下,Langmuir方程及准二级动力学模型能够更好地拟合吸附过程。拟合结果显示OS-600理论Cd^(2+)最大吸附量为9.04 mg/g,Pb^(2+)最大吸附量为44.84 mg/g。实测OS-600对Cd^(2+)、Pb^(2+)的实测吸附量分别为6.69、35.42 mg/g,分别高出OS原样吸附量的53.44%、71.69%。OS半焦温度以400~700℃为宜,半焦时间不低于2 h,研究结果为半焦OS制备吸附材料时温度条件优化提供了理论支撑。

Dip2a regulates stress susceptibility in the basolateral amygdala

Dysregulation of neurotransmitter metabolism in the central nervous system contributes to mood disorders such as depression, anxiety, and post–traumatic stress disorder. Monoamines and amino acids are important types of neurotransmitters. Our previous results have shown that disco-interacting protein 2 homolog A(Dip2a) knockout mice exhibit brain development disorders and abnormal amino acid metabolism in serum. This suggests that DIP2A is involved in the metabolism of amino acid–associated neurotransmitters. Therefore, we performed targeted neurotransmitter metabolomics analysis and found that Dip2a deficiency caused abnormal metabolism of tryptophan and thyroxine in the basolateral amygdala and medial prefrontal cortex. In addition, acute restraint stress induced a decrease in 5-hydroxytryptamine in the basolateral amygdala. Additionally, Dip2a was abundantly expressed in excitatory neurons of the basolateral amygdala, and deletion of Dip2a in these neurons resulted in hopelessness-like behavior in the tail suspension test. Altogether, these findings demonstrate that DIP2A in the basolateral amygdala may be involved in the regulation of stress susceptibility. This provides critical evidence implicating a role of DIP2A in affective disorders.

Interfacial stress engineering toward enhancement of ferroelectricity in Al doped HfO_(2) thin films

Ferroelectric HfO_(2)has attracted much attention owing to its superior ferroelectricity at an ultra-thin thickness and good compatibility with Si-based complementary metal-oxide-semiconductor(CMOS)technology.However,the crystallization of polar orthorhombic phase(o-phase)HfO_(2)is less competitive,which greatly limits the ferroelectricity of the as-obtained ferroelectric HfO_(2)thin films.Fortunately,the crystallization of o-phase HfO_(2)can be thermodynamically modulated via interfacial stress engineering.In this paper,the growth of improved ferroelectric Al doped HfO_(2)(HfO_(2):Al)thin films on(111)-oriented Si substrate has been reported.Structural analysis has suggested that nonpolar monoclinic HfO_(2):Al grown on(111)-oriented Si substrate suffered from a strong compressive strain,which promoted the crystallization of(111)-oriented o-phase HfO_(2)in the as-grown HfO_(2):Al thin films.In addition,the in-plane lattice of(111)-oriented Si substrate matches well with that of(111)-oriented o-phase HfO_(2),which further thermally stabilizes the o-phase HfO_(2).Accordingly,an improved ferroelectricity with a remnant polarization(2P_(r))of 26.7C/cm^(2) has been obtained.The results shown in this work provide a simple way toward the preparation of improved ferroelectric HfO_(2)thin films.

Upregulation of α-ENaC induces pancreatic β-cell dysfunction,ER stress,and SIRT2 degradation

Islet beta cells(β-cells)produce insulin in response to high blood glucose levels,which is essential for preserving glucose homeostasis.Voltage-gated ion channels inβ-cells,including Na+,K+,and Ca2+channels,aid in the release of insulin.The epithelial sodium channel alpha subunit(α-ENaC),a voltage-independent sodium ion channel,is also expressed in human pancreatic endocrine cells.However,there is no reported study on the function of ENaC in theβ-cells.In the current study,we found thatα-ENaC was expressed in human pancreatic glandule and pancreatic isletβ-cells.In the pancreas of db/db mice and high-fat diet-induced mice,and in mouse isletβ-cells(MIN6 cells)treated with palmitate,α-ENaC expression was increased.Whenα-ENaC was overexpressed in MIN6 cells,insulin content and glucose-induced insulin secretion were significantly reduced.On the other hand,palmitate injured isletβ-cells and suppressed insulin synthesis and secretion,but increasedα-ENaC expression in MIN6 cells.However,α-ENaC knockout(Scnn1a−/−)in MIN6 cells attenuatedβ-cell disorder induced by palmitate.Furthermore,α-ENaC regulated the ubiquitylation and degradation of sirtuin 2 inβ-cells.α-ENaC also modulatedβ-cell function in correlation with the inositol-requiring enzyme 1 alpha/X-box binding protein 1(IRE1α/XBP1)and protein kinase RNA-like endoplasmic reticulum kinase/C/EBP homologous protein(PERK/CHOP)endoplasmic reticulum stress pathways.These results suggest thatα-ENaC may play a novel role in insulin synthesis and secretion in theβ-cells,and the upregulation ofα-ENaC promotes isletβ-cell dysfunction.In conclusion,α-ENaC may be a key regulator involved in isletβ-cell damage and a potential therapeutic target for type 2 diabetes mellitus.

Hesperidin ameliorates H_(2)O_(2)-induced bovine mammary epithelial cell oxidative stress via the Nrf2 signaling pathway

Background Hesperidin is a citrus flavonoid with anti-inflammatory and antioxidant potential. However, its protective effects on bovine mammary epithelial cells(b MECs) exposed to oxidative stress have not been elucidated.Results In this study, we investigated the effects of hesperidin on H_(2)O_(2)-induced oxidative stress in b MECs and the underlying molecular mechanism. We found that hesperidin attenuated H_(2)O_(2)-induced cell damage by reducing reactive oxygen species(ROS) and malondialdehyde(MDA) levels, increasing catalase(CAT) activity, and improving cell proliferation and mitochondrial membrane potential. Moreover, hesperidin activated the Keap1/Nrf2/ARE signaling pathway by inducing the nuclear translocation of Nrf2 and the expression of its downstream genes NQO1 and HO-1, which are antioxidant enzymes involved in ROS scavenging and cellular redox balance. The protective effects of hesperidin were blocked by the Nrf2 inhibitor ML385, indicating that they were Nrf2 dependent.Conclusions Our results suggest that hesperidin could protect b MECs from oxidative stress injury by activating the Nrf2 signaling pathway, suggesting that hesperidin as a natural antioxidant has positive potential as a feed additive or plant drug to promote the health benefits of bovine mammary.

BTG2 interference ameliorates high glucose-caused oxidative stress, cell apoptosis, and lipid deposition in HK-2 cells

Objective:Diabetic nephropathy(DN)is a deleterious microangiopathy of diabetes,constituting a critical determinant of fatality in diabetic patients.This work is purposed to disclose the effects and modulatory mechanism of BTG anti-proliferation factor 2(BTG2)during the pathological process of DN.Methods:BTG2 expression in kidney tissues of diabetic mice and high glucose(HG)-exposed human proximal tubular cell line HK-2 was assessed with Western blot and RT-qPCR.The diabetic mice model was constructed by streptozotocin injection and confirmed by the blood glucose level beyond 16.7 mmol/L.Hematoxylin and eosin(H&E)staining and measurement of kidney function hallmarks were conducted to assess kidney injury.Cell counting kit(CCK)-8 method and TUNEL assay appraised cell activity and apoptosis.Oil red O staining assayed lipid accumulation.Relevant commercial kits were used to estimate oxidative stress-related factors.Co-immunoprecipitation(Co-IP)assay testified the binding relationship of BTG2 with protein arginine methyltransferase 1(PRMT1).Results:BTG2 expression was significantly raised in renal tissues of diabetic mice and HK-2 cells exposed to HG.BTG2 deficiency improved viability and extenuated the apoptosis,lipid deposition as well as oxidative stress in HK-2 cells following HG exposure.In addition,PRMT1 was also overexpressed in HK-2 cells exposed to HG.BTG2 interacted with PRMT1 and positively modulated PRMT1 expression.The effects of BTG2 interference on viability,apoptosis,lipid deposition,and oxidative stress in HG-challenged HK-2 cells were partially abrogated by PRMT1 overexpression.Conclusion:Altogether,BTG2 might aggravate HK-2 cell injury in response to HG by binding with PRMT1,providing a novel target for the therapeutic strategy of DN.

8-Hydroxy-2'-Deoxyguanosine (8-OH-2dG) as a Biomarker of Oxidative Stress (OS) in the Acute Exacerbation of Spontaneous Preterm Birth (SPTB)

Spontaneous preterm birth (SPTB) is characterized by the delivery of a baby before 37 completed weeks of gestation, and this condition is associated with significant health challenges for the newborn. Emerging evidence highlights the importance of biomarkers for understanding the mechanisms underlying SPTB. One such biomarker, 8-OH-2dG, plays a critical role in evaluating oxidative stress and its impact on pregnancy outcomes. It has been demonstrated that 8-OH-2dG is a product of oxidative DNA damage and is widely recognized as a key indicator of cellular oxidative stress. Elevated reactive oxygen species in SPTB result in higher levels of the DNA degradation product 8-OH-2dG in amniotic fluid, causing damage to maternal and fetal tissues that could lead to premature rupture of fetal membranes. Therefore, evaluating the role of 8-OH-2dG in SPTB is of great interest. This review provides an overview of the current knowledge on 8-OH-2dG as a biomarker for SPTB and aims to elucidate its mechanism in this condition.

Oxidative stress mediates glycidol-induced endothelial injury and its protection by 6-C-(E-2-fluorostyryl)naringenin

Glycidol is a common lipid-derived foodborne toxicant mainly presents in refined oils and related foodstuffs.Vascular endothelial cells may be potential targets of the deleterious effects associated with glycidol exposure.In human umbilical vein endothelial cells(HUVECs),we found that glycidol treatment promoted endothelialto-mesenchymal transition(EndMT)at a lower concentration(0.5 mmol/L),while induced apoptosis and inflammation at a higher concentration(1 mmol/L).These harmful effects were achieved by the activation of NF-κB/MAPK signaling pathway and were mediated by reactive oxygen species(ROS).In addition,the protective potential of 6-C-(E-2-fluorostyryl)naringenin(6-CEFN)against glycidol was evaluated and compared with naringenin.HUVECs pre-treated with 6-CEFN,but not naringenin,displayed resistance to endothelial dysfunction caused by glycidol.